Bordetella pertussis infection of human monocytes inhibits antigen-dependent CD4 T cell proliferation

J Infect Dis. 1997 Sep;176(3):678-86. doi: 10.1086/514090.


Human monocytes and macrophages bind Bordetella pertussis through multiple specific receptor-ligand interactions; however, the effect of these interactions on monocyte and macrophage function is not well understood. In an in vitro system, B. pertussis infection of human monocytes significantly impaired T cell proliferation to exogenous antigen at MOIs as low as 1.0. B. pertussis isogenic mutant strains deficient in filamentous hemagglutinin or adenylate cyclase toxin were incapable of proliferation inhibition, suggesting that these virulence-associated factors are essential for this activity. B. pertussis-induced monocyte death alone did not explain these results, nor did differences in intracellular survival. In addition, B. pertussis infection did not significantly alter monocyte phagocytosis of complement-opsonized latex particles, indicating that B. pertussis infection does not globally impair monocyte functions in this system. These results suggest that B. pertussis may be capable of subverting cellular immune defenses in an infected host.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenylate Cyclase Toxin
  • Adhesins, Bacterial / immunology
  • Antigen Presentation
  • Bordetella pertussis / immunology
  • Bordetella pertussis / pathogenicity
  • Bordetella pertussis / physiology*
  • CD4-Positive T-Lymphocytes / immunology*
  • Cell Death
  • Cell Division
  • Complement System Proteins
  • Heating
  • Hemagglutinins / immunology
  • Humans
  • Kinetics
  • Monocytes / immunology
  • Monocytes / microbiology*
  • Tetanus Toxoid / immunology
  • Virulence
  • Virulence Factors, Bordetella / immunology


  • Adenylate Cyclase Toxin
  • Adhesins, Bacterial
  • Hemagglutinins
  • Tetanus Toxoid
  • Virulence Factors, Bordetella
  • filamentous hemagglutinin adhesin, Bordetella pertussis
  • Complement System Proteins